On June 21, 1990, 11 days after returning from the Grand
Canyon North Rim (GCNR), a 61-year-old California resident
developed an acute illness lasting 2 days, characterized by
fever, shaking chills, headache, myalgias, and drenching
sweats. During the next 2 weeks, he had three febrile relapses
and was hospitalized. Physical examination and laboratory
studies were nondiagnostic. However, during a fourth
recurrence of fever and prostration, examination of a
peripheral blood smear revealed spirochetes, consistent with
the diagnosis of relapsing fever. The patient was treated with
tetracycline and recovered.

One additional confirmed case with onset July 5 and one
suspected case with onset July 12 were reported in Arizona
residents. All three patients had stayed overnight in cabins
at the GCNR.

Beginning July 6, 1990, visitors to the GCNR were notified
of the risk for exposure to tickborne relapsing fever (TBRF).
A survey of 244 employees at the GCNR identified two persons
who had had recurrent febrile symptoms compatible with TBRF.
One had been hospitalized with meningismus and cerebrospinal
fluid pleocytosis. A retrospective mail and telephone survey
of 6993 visitor groups, representing more than 10,000 persons
who stayed in park cabins during the 1990 season, identified
14 cases of laboratory-confirmed (four cases) or clinically
defined (10 cases) relapsing fever* in park visitors from nine
states, Canada, and Germany. Seven of the 14 patients had been
hospitalized.

Editorial Note

Editorial Note:

This outbreak is the first recognized occurrence of TBRF at
GCNR since 1973, when an interstate outbreak of 62 confirmed
or suspected cases occurred in employees or visitors who had
stayed in cabins at GCNR (1). TBRF is endemic throughout much
of the western United States; sporadic cases occur each summer
and fall. The disease is caused by infection with the
spirochetes Borrelia hermsii or B. turicatae; B. hermsii was
identified in 1973 at the GCNR (1). The soft ticks of the
genus Ornithodoros, which transmit the illness, usually feed
on rodents and frequently infest rodent nesting material (2).
The ticks are reclusive, usually feeding at night for only
5-20 minutes. Their bites are painless and frequently go
unnoticed (3). Most infections with B. hermsii are acquired by
persons vacationing in mountain cabins where rodents have
nested (1-7).

Because onset of illness occurs 4-18 days after infection,
patients infected with TBRF in tourist areas where the disease
is endemic often develop symptoms after they have returned to
areas where TBRF is not suspected. TBRF that is undiagnosed
and untreated may cause recurrent febrile illness for weeks to
months before the illness resolves. Neurologic sequelae, such
as aseptic meningitis and cranial nerve palsy, occur in a
small proportion of patients. Serologic testing by
enzyme-linked immunosorbent assay is available at CDC's
Division of Vector-Borne Infectious Diseases, Center for
Infectious Diseases, through state health departments and may
aid with a diagnosis when symptoms are suggestive of TBRF but
laboratory results are equivocal. Following infection, paired
serum specimens often demonstrate diagnostic levels of
antibody to B. hermsii or B. turicatae.

The 1973 outbreak was associated with epizootic plague
(2,4), which caused a marked decrease in rodent populations
that serve as the usual hosts for the vector tick and resulted
in increased feeding of ticks on humans. Recent observations
suggest that a decline in rodent populations occurred in 1990,
which may similarly have increased the risk for human
exposure.

Prevention strategies for TBRF focus on avoiding tick bites
and preventing rodents from nesting in human shelters in areas
where TBRF is endemic. "Rodent proofing"--structural changes
that prevent rodent access to the foundations or attics of
homes and vacation cabins--reduces human contact with ticks
that transmit the disease.

weeks of exposure in any person who had been a resident or
overnight visitor at the GCNR from May 15 through August 15,
1990, from whom spirochetes were visualized on a Wright- or
Giemsa-stained blood smear, or in whom antibody to Borrelia
hermsii was demonstrated by enzyme-linked immunosorbent assay.
A clinical case was defined as illness in a resident or
visitor during the same dates who had fever and three of four
characteristic symptoms (chills, sweats, myalgias, or
headache) and in whom a history of clinical remission followed
by relapse was reported.

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